학술논문

Brain arteriolosclerosis
Document Type
article
Source
Acta Neuropathologica. 141(1)
Subject
Biomedical and Clinical Sciences
Neurosciences
Aging
Brain Disorders
Acquired Cognitive Impairment
Alzheimer's Disease Related Dementias (ADRD)
Dementia
Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD)
Alzheimer's Disease
Neurodegenerative
Vascular Cognitive Impairment/Dementia
2.1 Biological and endogenous factors
Aetiology
Neurological
Mental health
Aged
Aged
80 and over
Animals
Arterioles
Brain
Cerebral Amyloid Angiopathy
Cognition Disorders
Humans
Intracranial Arteriosclerosis
Neuroimaging
SVD
Arteriosclerosis
cAVU
Senescence
Neuropathology
Clinical Sciences
Neurology & Neurosurgery
Language
Abstract
Brain arteriolosclerosis (B-ASC), characterized by pathologic arteriolar wall thickening, is a common finding at autopsy in aged persons and is associated with cognitive impairment. Hypertension and diabetes are widely recognized as risk factors for B-ASC. Recent research indicates other and more complex risk factors and pathogenetic mechanisms. Here, we describe aspects of the unique architecture of brain arterioles, histomorphologic features of B-ASC, relevant neuroimaging findings, epidemiology and association with aging, established genetic risk factors, and the co-occurrence of B-ASC with other neuropathologic conditions such as Alzheimer's disease and limbic-predominant age-related TDP-43 encephalopathy (LATE). There may also be complex physiologic interactions between metabolic syndrome (e.g., hypertension and inflammation) and brain arteriolar pathology. Although there is no universally applied diagnostic methodology, several classification schemes and neuroimaging techniques are used to diagnose and categorize cerebral small vessel disease pathologies that include B-ASC, microinfarcts, microbleeds, lacunar infarcts, and cerebral amyloid angiopathy (CAA). In clinical-pathologic studies that factored in comorbid diseases, B-ASC was independently associated with impairments of global cognition, episodic memory, working memory, and perceptual speed, and has been linked to autonomic dysfunction and motor symptoms including parkinsonism. We conclude by discussing critical knowledge gaps related to B-ASC and suggest that there are probably subcategories of B-ASC that differ in pathogenesis. Observed in over 80% of autopsied individuals beyond 80 years of age, B-ASC is a complex and under-studied contributor to neurologic disability.